Synaptic transmission in sympathetic vasoconstrictor pathways and its modification after injuries

The discharge of vasoconstrictor pathways arising in the CNS is largely unmodified as it passes through the sympathetic ganglia to the vasculature. The underlying synaptic events have been revealed by intracellular recordings from sympathetic paravertebral ganglion cells in the course of ongoing and reflex activity in anesthetized animals, first made in Skok’s Laboratory in Kyiv (Ukraine). Each preganglionic neuron diverges to contact a number of post-ganglionic neurons, on each of which several pre-ganglionic inputs converge. However, only suprathreshold “strong,” or “dominant” synapses are effective in transmitting the CNS signals. Strong synapses differ from the other subthreshold “weak,” or “accessory” inputs: (a) excitatory synaptic currents are >1 nA in their amplitude, (b) 3 to ≈>30 times more quanta of acetylcholine are released, (c) pre-synaptic Ca²⁺ entry through channels resistant to all-known antagonists triggers acetylcholine release, and (d) post-synaptic Ca²⁺ entry boosts and prolongs the nicotinic current. While the majority of postganglionic neurons have only one strong input, a proportion receives two or, rarely, three such inputs. In cells with multiple strong inputs, an equivalent number of discrete Ca²⁺ currents can be evoked at distinct foci electrically distant from the soma, suggesting that each strong input has a unique dendritic association with a cluster of Ca²⁺ channels. When strong preganglionic inputs are destroyed, residual weak synapses sprout and rapidly restore the suprathreshold connections. While much remains to be discovered about how strong synapses are established, their high safety factor ensures the wide and secure distribution of vasoconstrictor command signals from the CNS. Neirofiziologiya/Neurophysiology, Vol. 39, Nos. 4/5, pp. 294–301, July–October, 2007.